MiR-212-3p inhibits LPS-induced inflammatory response through targeting HMGB1 in murine macrophages

Experimental Cell Research

Volumn 350, Issue 2, 2017, Pages 318-326

  Chen, Weiwei ^a   Ma, Xiaoying ^a   Zhang, Peng ^a   Li, Qifeng ^b   Liang, Xin ^a   Liu, Jianwen ^a  

^a EAST CHINA UNIVERSITY OF SCIENCE AND TECHNOLOGY   (China)

^b SHANGHAI JIAO TONG UNIVERSITY SCHOOL OF MEDICINE   (China)

Author keywords

HMGB1; Inflammatory response; MAPKs; MiR 212 3p

Indexed keywords

HIGH MOBILITY GROUP B1 PROTEIN; INTERLEUKIN 6; LIPOPOLYSACCHARIDE; MICRORNA; MICRORNA 212 3P; TUMOR NECROSIS FACTOR; UNCLASSIFIED DRUG; MIRN212 MICRORNA, MOUSE;

3' UNTRANSLATED REGION; ANIMAL CELL; ARTICLE; BIOINFORMATICS; CYTOKINE PRODUCTION; CYTOPLASM; DOWN REGULATION; ENZYME LINKED IMMUNOSORBENT ASSAY; ENZYME PHOSPHORYLATION; GENE OVEREXPRESSION; GENE SILENCING; GENETIC TRANSFECTION; INNATE IMMUNITY; LUCIFERASE ASSAY; MICROARRAY ANALYSIS; MOUSE; NONHUMAN; PREDICTION; PRIORITY JOURNAL; QUANTITATIVE ANALYSIS; RAW 264.7 CELL LINE; REAL TIME POLYMERASE CHAIN REACTION; UPREGULATION; WESTERN BLOTTING; ANIMAL; CELL LINE; DRUG EFFECTS; GENETICS; INFLAMMATION; MACROPHAGE; METABOLISM; SIGNAL TRANSDUCTION;

ANIMALS; CELL LINE; HMGB1 PROTEIN; INFLAMMATION; INTERLEUKIN-6; LIPOPOLYSACCHARIDES; MACROPHAGES; MAP KINASE SIGNALING SYSTEM; MICE; MICRORNAS; TUMOR NECROSIS FACTOR-ALPHA;

EID: 85008173897     PISSN: 00144827     EISSN: 10902422     Source Type: Journal    
DOI: 10.1016/j.yexcr.2016.12.008     Document Type: Article

References (41)

1. [1] Angus, D.C., Linde-Zwirble, W.T., Lidicker, J., Clermont, G., Carcillo, J., Pinsky, M.R., Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit. Care Med. 29 (2001), 1303–1310.
2. [2] Levy, M.M., Artigas, A., Phillips, G.S., Rhodes, A., Beale, R., Osborn, T., Vincent, J.-L., Townsend, S., Lemeshow, S., Dellinger, R.P., Outcomes of the Surviving Sepsis Campaign in intensive care units in the USA and Europe: a prospective cohort study. Lancet Infect. Dis. 12 (2012), 919–924.
3. [3] Harbarth, S., Holeckova, K., Froidevaux, C., Pittet, D., Ricou, B., Grau, G.E., Vadas, L., Pugin, J., Diagnostic Value of Procalcitonin, Interleukin-6, and Interleukin-8 in Critically Ill patients admitted with suspected sepsis. Am. J. Respir. Crit. Care Med. 164 (2001), 396–402.
4. [4] Bozza, F.A., Salluh, J.I., Japiassu, A.M., Soares, M., Assis, E.F., Gomes, R.N., Bozza, M.T., Castro-Faria-Neto, H.C., Bozza, P.T., Cytokine profiles as markers of disease severity in sepsis: a multiplex analysis. Crit. Care, 11, 2007, R49.
5. [5] Bossink, A.W., Paemen, L., Jansen, P.M., Hack, C.E., Thijs, L.G., Van Damme, J., Plasma levels of the chemokines monocyte chemotactic proteins-1 and -2 are elevated in human sepsis. Blood, 86, 1995, 3841.
6. [6] Simon, L., Gauvin, F., Amre, D.K., Saint-Louis, P., Lacroix, J., Serum procalcitonin and C-reactive protein levels as markers of bacterial infection: a systematic review and meta-analysis. Clin. Infect. Dis. 39 (2004), 206–217.
7. [7] Essandoh, K., Fan, G.C., Role of extracellular and intracellular microRNAs in sepsis. Biochim. Et. Biophys. Acta 1842 (2014), 2155–2162.
8. [8] Peters, K., Molecular basis of endothelial dysfunction in sepsis. Cardiovasc. Res. 60 (2003), 49–57.
9. [9] Beutler, B.A., TLRs and innate immunity. Blood, 113, 2009, 1399.
10. [10] Musumeci, D., Roviello, G.N., Montesarchio, D., An overview on HMGB1 inhibitors as potential therapeutic agents in HMGB1-related pathologies. Pharmacol. Ther. 141 (2014), 347–357.
11. [11] Bustin, M., Regulation of DNA-dependent activities by the functional motifs of the high-mobility-Group chromosomal proteins. Mol. Cell. Biol. 19 (1999), 5237–5246.
12. [12] Bianchi, M.E., Beltrame, M., Upwardly mobile proteins. EMBO Rep., 1, 2000, 109.
13. [13] Wang, H., Yang, H., Tracey, K.J., Extracellular role of HMGB1 in inflammation and sepsis. J. Intern. Med. 255 (2004), 320–331.
14. [14] Hsieh, C.H., Rau, C.S., Jeng, S.F., Lin, C.J., Chen, Y.C., Wu, C.J., Lu, T.H., Lu, C.H., Chang, W.N., Identification of the potential target genes of microRNA-146a induced by PMA treatment in human microvascular endothelial cells. Exp. Cell Res. 316 (2010), 1119–1126.
15. [15] Ardekani, A.M., Naeini, M.M., The role of MicroRNAs in human diseases, Avicenna. J. Med. Biotechnol. 2 (2010), 161–179.
16. [16] Zhu, Q.Y., Liu, Q., Chen, J.X., Lan, K., Ge, B.X., MicroRNA-101 targets MAPK phosphatase-1 to regulate the activation of MAPKs in macrophages. J. Immunol. 185 (2010), 7435–7442.
17. [17] Wei, J., Huang, X., Zhang, Z., Jia, W., Zhao, Z., Zhang, Y., Liu, X., Xu, G., MyD88 as a target of microRNA-203 in regulation of lipopolysaccharide or Bacille Calmette-Guerin induced inflammatory response of macrophage RAW264.7 cells. Mol. Immunol. 55 (2013), 303–309.
18. [18] Jiang, P., Liu, R., Zheng, Y., Liu, X., Chang, L., Xiong, S., Chu, Y., MiR-34a inhibits lipopolysaccharide-induced inflammatory response through targeting Notch1 in murine macrophages. Exp. Cell Res. 318 (2012), 1175–1184.
19. [19] Li, M., Chen, H., Chen, L., Chen, Y., Liu, X., Mo, D., miR-709 modulates LPS-induced inflammatory response through targeting GSK-3beta. Int. Immunopharmacol. 36 (2016), 333–338.
20. [20] Niu, Y., Mo, D., Qin, L., Wang, C., Li, A., Zhao, X., Wang, X., Xiao, S., Wang, Q., Xie, Y., He, Z., Cong, P., Chen, Y., Lipopolysaccharide-induced miR-1224 negatively regulates tumour necrosis factor-alpha gene expression by modulating Sp1. Immunology 133 (2011), 8–20.
21. [21] Xu, G., Zhang, Z., Xing, Y., Wei, J., Ge, Z., Liu, X., Zhang, Y., Huang, X., MicroRNA-149 negatively regulates TLR-triggered inflammatory response in macrophages by targeting MyD88. J. Cell. Biochem. 115 (2014), 919–927.
22. [22] Tili, E., Michaille, J.J., Cimino, A., Costinean, S., Dumitru, C.D., Adair, B., Fabbri, M., Alder, H., Liu, C.G., Calin, G.A., Croce, C.M., Modulation of miR-155 and miR-125b levels following Lipopolysaccharide/TNF- stimulation and their possible roles in regulating the response to endotoxin shock. J. Immunol. 179 (2007), 5082–5089.
23. [23] Xu, K., Liang, X., Cui, D., Wu, Y., Shi, W., Liu, J., MiR-1915 inhibits Bcl-2 to modulate multidrug resistance by increasing drug-sensitivity in human colorectal carcinoma cells. Mol. Carcinog. 52 (2013), 70–78.
24. [24] Maracle, C.X., Kucharzewska, P., Helder, B., van der Horst, C., Correa de Sampaio, P., Noort, A.R., van Zoest, K., Griffioen, A.W., Olsson, H., Tas, S.W., Targeting non-canonical nuclear factor-kappaB signalling attenuates neovascularization in a novel 3D model of rheumatoid arthritis synovial angiogenesis. Rheumatology, 2016.
25. [25] Nahid, M.A., Satoh, M., Chan, E.K., MicroRNA in TLR signaling and endotoxin tolerance. Cell. Mol. Immunol. 8 (2011), 388–403.
26. [26] Park, J.S., Gamboni-Robertson, F., He, Q., Svetkauskaite, D., Kim, J.-Y., Strassheim, D., Sohn, J.-W., Yamada, S., Maruyama, I., Banerjee, A., Ishizaka, A., Abraham, E., High mobility group box 1 protein interacts with multiple Toll-like receptors. Am. J. Physiol. - Cell Physiol., 290, 2006, C917.
27. [27] O'Connell, R.M., Rao, D.S., Chaudhuri, A.A., Baltimore, D., Physiological and pathological roles for microRNAs in the immune system. Nat. Rev. Immunol. 10 (2010), 111–122.
28. [28] Baltimore, D., Boldin, M.P., O'Connell, R.M., Rao, D.S., Taganov, K.D., MicroRNAs: new regulators of immune cell development and function. Nat. Immunol. 9 (2008), 839–845.
29. [29] Nahid, M.A., Yao, B., Dominguez-Gutierrez, P.R., Kesavalu, L., Satoh, M., Chan, E.K., Regulation of TLR2-mediated tolerance and cross-tolerance through IRAK4 modulation by miR-132 and miR-212. J. Immunol. 190 (2013), 1250–1263.
30. [30] Park, J.K., Henry, J.C., Jiang, J., Esau, C., Gusev, Y., Lerner, M.R., Postier, R.G., Brackett, D.J., Schmittgen, T.D., miR-132 and miR-212 are increased in pancreatic cancer and target the retinoblastoma tumor suppressor. Biochem. Biophys. Res. Commun. 406 (2011), 518–523.
31. [31] Wu, R., Li, F., Zhu, J., Tang, R., Qi, Q., Zhou, X., Li, R., Wang, W., Hua, D., Chen, W., A functional variant at miR-132-3p, miR-212-3p, and miR-361-5p binding site in CD80 gene alters susceptibility to gastric cancer in a Chinese Han population. Med. Oncol., 31, 2014, 60.
32. [32] Ding, G., Zhou, L., Qian, Y., Fu, M., Chen, J., Chen, J., Xiang, J., Wu, Z., Jiang, G., Cao, L., Pancreatic cancer-derived exosomes transfer miRNAs to dendritic cells and inhibit RFXAP expression via miR-212-3p. Oncotarget 6 (2015), 29877–29888.
33. [33] Liu, H., Li, C., Shen, C., Yin, F., Wang, K., Liu, Y., Zheng, B., Zhang, W., Hou, X., Chen, X., Wu, J., Wang, X., Zhong, C., Zhang, J., Shi, H., Ai, J., Zhao, S., MiR-212-3p inhibits glioblastoma cell proliferation by targeting SGK3. J. neuro-Oncol. 122 (2015), 431–439.
34. [34] Ci, X., Ren, R., Xu, K., Li, H., Yu, Q., Song, Y., Wang, D., Li, R., Deng, X., Schisantherin A exhibits anti-inflammatory properties by down-regulating NF-kappaB and MAPK signaling pathways in lipopolysaccharide-treated RAW 264.7 cells. Inflammation 33 (2010), 126–136.
35. [35] Sha, Y., Zmijewski, J., Xu, Z., Abraham, E., HMGB1 develops enhanced proinflammatory activity by binding to cytokines. J. Immunol. 180 (2008), 2531–2537.
36. [36] Wang, X., Guo, Y., Wang, C., Yu, H., Yu, X., Yu, H., MicroRNA-142-3p Inhibits chondrocyte apoptosis and inflammation in osteoarthritis by targeting HMGB1. Inflammation 39 (2016), 1718–1728.
37. [37] Yao, L., Lv, X., Wang, X., MicroRNA 26a inhibits HMGB1 expression and attenuates cardiac ischemia-reperfusion injury. J. Pharmacol. Sci. 131 (2016), 6–12.
38. [38] Kim, S.R., Ha, Y.M., Kim, Y.M., Park, E.J., Kim, J.W., Park, S.W., Kim, H.J., Chung, H.T., Chang, K.C., Ascorbic acid reduces HMGB1 secretion in lipopolysaccharide-activated RAW 264.7 cells and improves survival rate in septic mice by activation of Nrf2/HO-1 signals. Biochem. Pharmacol. 95 (2015), 279–289.
39. [39] Kim, E.K., Choi, E.J., Pathological roles of MAPK signaling pathways in human diseases. Biochim. Et. Biophys. Acta 1802 (2010), 396–405.
40. [40] Fiuza, C., Bustin, M., Talwar, S., Tropea, M., Gerstenberger, E., Shelhamer, J.H., Suffredini, A.F., Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells. Blood 101 (2003), 2652–2660.
41. [41] Porto, A., Palumbo, R., Pieroni, M., Aprigliano, G., Chiesa, R., Sanvito, F., Maseri, A., Bianchi, M.E., Smooth muscle cells in human atherosclerotic plaques secrete and proliferate in response to high mobility group box 1 protein. FASEB J. 20 (2006), 2565–2566.